‘Wake up dear Prime Minister Muhyiddin Yassin – you are a self-proclaimed “abah” (father) that wishes to “rotan” (cane) his rakyat for misbehaving and not following standard operating procedure (SOP). You fail to realise that the saddening facts of this Covid-19 wave listed down above are not due to Covid-19, but rather the failure of your administration to prioritise the health of the rakyat above all else...’
Read here (Malaysiakini, Oct 11, 2020)
‘Donald Trump has clear risk factors - including his age, weight and being male - that all raise the chances of a severe coronavirus infection. He is 74 and has a Body Mass Index (BMI) over 30, which is the clinical definition of obesity. So now he has tested positive for the virus, what does it mean?’
Read here (BBC, Oct 2, 2020)
“Long Covid” was first used by Elisa Perego as a Twitter hashtag in May to describe her own experience of a multiphasic, cyclical condition that differed in time course and symptomatology from the bi-phasic pathway discussed in early scientific papers, which focused on hospitalized patients. Just three months later, following intense advocacy by patients across the world, this patient made term has been taken up by powerful actors, including the World Health Organization. Politicians have used it too: Matt Hancock, UK health secretary, recently explained to a parliamentary committee that “the impact of long covid can be really debilitating for a long period of time.”...
‘As patients and professionals, we see “Long Covid” as better able to navigate the socio-political, as well as clinical and public health challenges, posed by the pandemic in the coming months, for a number of reasons: (1) Long Covid acknowledges that cause and disease course are as yet unknown (2) Long Covid makes clear that “mild” covid-19 is not necessarily mild (3) Long Covid avoids “chronic,” “post” and “syndrome” (4)Long Covid draws attention to morbidity (5) Long Covid centres disabled people.
Read here (BMJ Opinion, Oct 1, 2020)
‘Last month, several college conferences, the Big Ten and the Pac 12 among them, postponed their sports seasons, including football, citing the risks posed to athletes by the coronavirus. A major factor in those decisions, according to some physicians, was the uncertain implications of a July paper in JAMA Cardiology. In this study of 100 people who had Covid-19, M.R.I.’s showed at least some signs of myocarditis in 60 of them, meaning they had inflammation in the heart muscle, which can weaken the organ and, on rare occasions, lead to sudden cardiac arrest. Another study, published this month in the same journal, looked at 26 Ohio State athletes who experienced Covid-19 with mild or no symptoms and detected evidence of possible myocarditis in five of them and lesser abnormalities in nine more. The condition poses a heightened risk to those whose physical activity puts stress on the heart: Even before the pandemic, myocarditis was a leading cause of death in young, otherwise healthy athletes.’
Read here (New York Times, Sept 23, 2020)
‘COVID-19 can cause worrying neurological symptoms like a loss of smell and taste, but Australian scientists are warning the damage the virus causes to the brain may also lead to more serious conditions such as Parkinson's disease.
‘It has happened before... Five years after the Spanish flu pandemic in the early 1900s, there was up to a three-fold increase in the incidence of Parkinson's disease. Kevin Barnham from the Florey Institute of Neuroscience and Mental Health said he believed a similar "silent wave" of neurological illness would follow this pandemic. "Parkinson's disease is a complex illness, but one of the causes is inflammation, and the virus helps to drive that inflammation," he said.’
Read here (ABC News, Sept 23, 2020)
‘Autopsies have found traces of the coronavirus’s genetic material in the heart, and actual viral particles within the heart’s muscle cells. Experiments have found that SARS-CoV-2 can destroy lab-grown versions of those cells. Several studies have now shown that roughly 10 to 30 percent of hospitalized COVID-19 patients had high levels of troponin—a protein released into the blood when the heart’s muscle cells are damaged. Such patients are more likely to die than others with no signs of heart injury.
‘This is worrying for people with severe symptoms, but more recently, a few studies suggested that COVID-19 can cause heart inflammation, or myocarditis, even in people who showed mild symptoms, or had recovered. These results were controversial but concerning. Myocarditis is frequently caused by viruses, and resolves on its own in many cases. But it can progress to more severe heart problems, and is one of the leading causes of sudden death in young adults. These studies contributed to decisions by two college football conferences—the Big Ten and the Pac-12—to cancel their fall season. (The Big Ten has since reversed its call, and the Pac-12 is considering doing the same)’
Read here (The Atlantic, Sept 21, 2020)
‘Covid-19 patients who are 80 or older are hundreds of times more likely to die than those under 40. That’s partly because they are more likely to have underlying conditions — like diabetes and lung disease — that seem to make the body more vulnerable to Covid-19.
‘But some scientists suggest another likely, if underappreciated, driver of this increased risk: the ageing immune system. The changes that ripple through our network of immune cells as the decades pass are complex, resulting in an overreaction here, a delayed response there and, overall, a strangely altered landscape of immunity.’
Read here (Today Online, Sept 13, 2020)
‘A survey in the Netherlands has suggested that most people who showed signs of having Covid-19 still had multiple symptoms nearly three months later. Only 0.7 per cent of respondents said they were completely symptom-free 79 days after first showing signs of infection, according to research published on Thursday in the European Respiratory Society’s Open Research journal. The survey is the first to show only a partial recovery among a large sample of people, according to the researchers. It involved more than 2,100 mostly non-hospitalised people confirmed or suspected to have had Covid-19 in the Netherlands and Flanders, the northern Dutch-speaking part of Belgium.’
Read here (South China Morning Post, Sept 11, 2020)
‘Different SARS-CoV-2 strains haven’t yet had a major impact on the course of the pandemic, but they might in future...
‘It’s even possible that the D614G change could make the virus an easier target for vaccines, Montefiori’s team found in a study posted to bioRxiv in July 13. Mice, monkeys and humans that received one of a number of experimental RNA vaccines, including one being developed by drug maker Pfizer in New York City, produced antibodies that proved more potent at blocking G viruses than D viruses.
‘With G viruses now ubiquitous, the finding is “good news”, says Montefiori. But as a scientist who has watched HIV mutate to elude many vaccines developed against it, he remains wary of the potential of SARS-CoV-2 to evade humanity’s responses. Luban agrees: “We need to keep our eyes open for additional changes.”
Read here (Nature, Sept 8, 2020)
‘As we head into fall, questions loom large about everything from reopening schools to the start of flu season. We’ve put together a guide to everything you need to know about this pandemic—be it how to keep your children entertained or how this outbreak is affecting the economy. We’ll be updating it regularly to help you keep track of all aspects of this rapidly evolving situation.’
Read here (Wired, Sept 4, 2020)
‘International clinical trials published on Wednesday confirm the hope that cheap, widely available steroid drugs can help seriously ill patients survive Covid-19, the illness caused by the coronavirus. Based on the new evidence, the World Health Organization issued new treatment guidance, strongly recommending steroids to treat severely and critically ill patients, but not to those with mild disease...
‘JAMA published that paper and three related studies, along with an editorial describing the research as an “important step forward in the treatment of patients with Covid-19.” Corticosteroids should now be the first-line treatment for critically ill patients, the authors said. The only other drug shown to be effective in seriously ill patients, and only modestly at that, is remdesivir. Steroids like dexamethasone, hydrocortisone and methylprednisolone are often used by doctors to tamp down the body’s immune system, alleviating inflammation, swelling and pain. Many Covid-19 patients die not of the virus, but of the body’s overreaction to the infection.’
Read here (New York Times, Sept 2, 2020)
WHO ‘living guidance' on corticosteroids for Covid-19:
Download here (WHO)
‘Earlier this summer, the Summit supercomputer at Oak Ridge National Lab in Tennessee set about crunching data on more than 40,000 genes from 17,000 genetic samples in an effort to better understand Covid-19. Summit is the second-fastest computer in the world, but the process — which involved analyzing 2.5 billion genetic combinations — still took more than a week.
‘When Summit was done, researchers analyzed the results. It was, in the words of Dr. Daniel Jacobson, lead researcher and chief scientist for computational systems biology at Oak Ridge, a “eureka moment.” The computer had revealed a new theory about how Covid-19 impacts the body: the bradykinin hypothesis. The hypothesis provides a model that explains many aspects of Covid-19, including some of its most bizarre symptoms. It also suggests 10-plus potential treatments, many of which are already FDA approved. Jacobson’s group published their results in a paper in the journal eLife in early July...
‘Covid-19 is like a burglar who slips in your unlocked second-floor window and starts to ransack your house. Once inside, though, they don’t just take your stuff — they also throw open all your doors and windows so their accomplices can rush in and help pillage more efficiently...’
Read here (Elemental Medium, September 1, 2020)
‘Yale researchers have identified significant differences in how the immune systems of women and men respond to the virus that causes COVID-19. In a study launched by Women’s Health Research at Yale and published Aug. 28 in Nature, the authors revealed possible biological explanations for why men are more likely than women to suffer severe cases of COVID-19 and die of the disease.
“We now have clear data suggesting that the immune landscape in COVID-19 patients is considerably different between the sexes and that these differences may underlie heightened disease susceptibility in men,” said senior author Akiko Iwasaki, the Waldemar Von Zedtwitz Professor of Immunobiology and Molecular, Cellar and Development Biology, and an investigator of the Howard Hughes Medical Institute. “Collectively, these data suggest we need different strategies to ensure that treatments and vaccines are equally effective for both women and men.”
Read here (Yale News, August 26, 2020)
‘Asymptomatic cases are not unique to Covid-19. They occur with the regular flu, and probably also featured in the 1918 pandemic, according to epidemiologist Neil Ferguson of Imperial College London. But scientists aren’t sure why certain people weather Covid-19 unscathed. “That is a tremendous mystery at this point,” says Donald Thea, an infectious disease expert at Boston University’s School of Public Health...
‘Disease tolerance is the ability of an individual, due to a genetic predisposition or some aspect of behavior or lifestyle, to thrive despite being infected with an amount of pathogen that sickens others... At least 90 percent of those infected with the tuberculosis bacterium don’t get sick. The same is true for many of the 1.5 billion of people globally who live with parasitic worms called helminths in their intestines...
‘...there are countless disease tolerance pathways. “Every time we figure one out, we find we have 10 more things we don’t understand,” King says. Things will differ with each disease, he adds, “so that becomes a bit overwhelming.”
‘Nevertheless, a growing number of experts agree that disease tolerance research could have profound implications for treating infectious disease in the future. Microbiology and infectious disease research has “all been focused on the pathogen as an invader that has to be eliminated some way,” says virologist Jeremy Luban of the University of Massachusetts Medical School. And as Ayres makes clear, he says, “what we really should be thinking about is how do we keep the person from getting sick.”
Read here (Scientific American, August 25, 2020)
‘Most statistics indicate that although cases of Covid-19 are rising in many parts of Europe and the United States, the number of deaths and cases of severe complications remain relatively low. For example, patients on ventilators have dropped from 3,000 at the epidemic’s peak in Britain to 70. At the same time, the number of cases in the UK have begun to rise in many areas.’
Questions: (1) What lies behind this trend? (2) Does that indicate that the worst may be over? (3) Is the Covid-19 virus becoming less deadly?
Read here (The Guardian, August 23, 2020)
‘The physical toll of long COVID almost always comes with an equally debilitating comorbidity of disbelief. Employers have told long-haulers that they couldn’t possibly be sick for that long. Friends and family members accused them of being lazy. Doctors refused to believe they had COVID-19. “Every specialist I saw—cardiologist, rheumatologist, dermatologist, neurologist—was wedded to this idea that ‘mild’ COVID-19 infections last two weeks,” says Angela Meriquez Vázquez, a children’s activist in Los Angeles. “In one of my first ER visits, I was referred for a psychiatric evaluation, even though my symptoms were of heart attack and stroke.”
Read here (The Atlantic, August 19, 2020)
‘The impact of COVID-19 on care home residents has been very different internationally, with some countries reporting no deaths (or infections) in care homes, such as Hong Kong, Jordan and Malta, and two countries reporting that over 80% of COVID-19 deaths were of care home residents. Without including the three countries with zero deaths, and with the caveat that the definitions used vary, on average the share of all COVID-19 deaths that were care home residents is 47% (based on 26 countries).’
Read here (International Long-term Care Policy Network, June 26, 2020)